Abstract:
:Tumor necrosis factor (TNF) actions in target tissues are mediated by various signalling pathways. The effect of TNF to stimulate resorption in fetal rat limb bones is not inhibited by indomethacin. The current studies were designed to assess the role of cyclic AMP (cAMP) and calcium as second messengers in this prostaglandin-independent action of TNF on bone resorption. TNF alone failed to increase cyclic AMP in fetal rat limb bones after either brief (15 min) or long-term (72 h) treatment. TNF-stimulated resorption in fetal rat limb bones was enhanced by the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX). In short term incubations, the combination of TNF + IBMX did not elicit increases in cAMP in the limb bones. In 72 h cultures, addition of IBMX revealed a dose-dependent effect of TNF to increase cAMP. TNF produced a significant increase in inositol phosphate turnover in limb bones, with a greater response at 5 min than at 1 or 20 min. The calcium channel blocker nitrendipine inhibited TNF-stimulated resorption in the fetal rat limb bones. TNF-stimulated resorption was attenuated by pretreatment with pertussis toxin (PTx). PTx did not inhibit the effect of TNF to increase inositol phosphate turnover. TNF did not increase cAMP, intracellular calcium, or inositol phosphates in the UMR-106 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
Bonejournal_title
Boneauthors
Shankar G,Stern PHdoi
10.1016/8756-3282(93)90317-4subject
Has Abstractpub_date
1993-11-01 00:00:00pages
871-6issue
6eissn
8756-3282issn
1873-2763pii
8756-3282(93)90317-4journal_volume
14pub_type
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